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17 beta-hydroxysteroid dehydrogenases--their role in pathophysiology
P Vihko1, P Härkönen, P Soronen
1Biocenter Oulu and Research Center for Molecular Endocrinology, University of Oulu, P.O. Box 5000, FIN-90014, Oulu, Finland. pvihko@whoccr.oulu.fi
Molecular and Cellular Endocrinology
|March 18, 2004
Summary
17 beta-Hydroxysteroid dehydrogenases (17HSDs) regulate sex hormone activity. Inhibiting 17HSD type 1 may treat estrogen-dependent breast cancer and impact prostate cancer progression.
Area of Science:
- Endocrinology
- Oncology
- Molecular Biology
Background:
- 17 beta-Hydroxysteroid dehydrogenases (17HSDs) interconvert active and less active sex steroid hormones.
- Estrogens are implicated in breast cancer, and androgens in prostate cancer.
- Estrogens may also contribute to cancers in non-traditional target tissues.
Purpose of the Study:
- To investigate changes in androgen and estrogen metabolism during prostate cancer progression.
- To explore the role of 17HSDs in both breast and prostate cancer.
- To assess the therapeutic potential of 17HSD inhibitors.
Main Methods:
- Utilized LNCaP prostate cancer cell lines to model cancer progression.
- Analyzed changes in steroid hormone metabolism in cultured cells.
- Examined the differential expression of 17HSD types in breast cancer cells.
Main Results:
- Prostate cancer progression in vitro involved significant alterations in sex hormone metabolism.
- Increased production of active estrogens was observed during LNCaP cell transformation.
- 17HSD type 1 activity was predominant in malignant breast cells, while type 2 was in non-malignant cells.
Conclusions:
- 17HSDs play a critical role in regulating hormone activity in cancer.
- Targeting 17HSD type 1 offers a potential therapeutic strategy for estrogen-dependent breast cancer.
- Estrogen metabolism is altered during prostate cancer progression, suggesting broader roles for estrogens in carcinogenesis.
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